Hydrogen Sulfide Mediates K and Na Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.

Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K, Na, and H in roots and effects of NaHS (a HS donor) on root ion fluxes in two contrasting poplar species, (salt-resistant) and (salt-sensitive). Both poplar species displayed a net K efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K efflux in roots irrespective of the duration of salt exposure, but K efflux was not pronounced in data collected from the LT salt stress treatment of . The NaCl-induced K efflux was inhibited by a K channel blocker, tetraethylammonium chloride (TEA) in root samples, but K loss increased with a specific inhibitor of plasma membrane (PM) H-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K loss was through depolarization-activated K channels. NaHS caused increased Na efflux and a corresponding increase in H influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H influx was not significant in samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na/H antiporter inhibitor) effectively inhibited the NaHS-augmented Na efflux, indicating that the HS-enhanced Na efflux was due to active Na exclusion across the PM. We therefore conclude that the beneficial effects of HS probably arise from upward regulation of the Na/H antiport system (H pumps and Na/H antiporters), which promote exchange of Na with H across the PM and simultaneously restricted the channel-mediated K loss that activated by membrane depolarization.